Corticosteroids: Management of Iatrogenic Cushing's Syndrome

Mary Carter, 49, an African-American woman, was diagnosed with systemic lupus erythematosus (SLE, or lupus) 20 years ago. For the first 10 years, her symptoms were confined mainly to her joints. The pain and swelling were controlled with NSAIDs and Plaquenil® (hydroxychloroquine sulfate, Sanofi) and she was able to lead a fairly active lifestyle. She taught second grade, cared for her two children and husband and loved to garden on weekends.

About 10 years ago, however, her condition worsened rapidly. She developed lupus-related pericarditis. She was started on prednisone 60 mg alternate day therapy, but after a month with little change in her cardiac symptoms, the drug was prescribed daily in the a.m. During the year Mary was maintained on prednisone, she developed steroid-induced diabetes, had frequent mood swings, a weight gain of 25 pounds distributed primarily in her abdomen and significant muscle wasting in her lower extremities.

Besides the decline in her physical health from the lupus, the side effects from the steroids caused Mary to become dissatisfied with her body image. In fact, after she had to take a leave of absence from teaching, she withdrew from almost all social activities. "I look like an ostrich.. - I have skinny legs, a big belly and a puffy face," she would frequently lament to her family.

MAINSTAY OF LUPUS TREATMENT

Lupus is a chronic autoimmune disease that causes inflammation of various parts of the body, especially the skin, joints, blood and kidneys. The form of lupus that affects multiple organ systems is known as SLE - some experts now believe it may be several diseases characterized by frequent flare-ups and remissions that may take as long as 7-10 years to diagnose.

Although there are many SLE patients who benefit from select immunosuppressive and cytotoxic drugs, corticosteroids are the mainstay of treatment. While debilitating side effects and secondary problems are associated with corticosteroids, experience in treating patients has resulted in preventing some of them.

Corticosteroids were first used in clinical practice in 1949 for the treatment of rheumatoid arthritis.1 Since then the indications for their use have spanned multiple specialties and organ systems including dermatology, rheumatology, immunology and oncology. The number of clinical conditions for which corticosteroids are indicated is extensive (see Table 1).

Table 1: Indications for Steroid Use (Partial Listing)1
Collagen Diseases
 systemic lupus erythematosus (SLE)
 mixed connective tissue disease
 scleroderma
Rheumatoid Disorders and Various Types of Arthritis
 osteoarthritis
 rheumatoid
 gout
 posttraumatic
Inflammatory Bowel Disease
 ulcerative colitis
 Crohn's disease
Inflammatory Dermatologic Disorders
 dermatitis
 psoriasis
Hematologic Disorders
 idiopathic thrombocytopenia purpura
Oncology
 Hodgkin's
 leukemia
 lymphoma
Respiratory Chronic Diseases
 COPD
 sarcoidosis
Organ Transplants
 prevent and treat rejections
Spinal Cord Injuries
 immediate post trauma swelling
Antenatal
 prevention of chronic lung disease in pre-term neonates; contraindicated post-natally
Allergic Conditions
 asthma
Inflammatory Ophthalmic Problems
Pain Management
Meningitis
Alcoholic Hepatitis

MIMIC ENDOGENOUS STEROIDS

More than 30 different steroids have been isolated from the adrenal cortex, but only two of these are of major importance to the endocrine functions of the body - the mineralocorticoids (aldosterone) and the glucocorticoids (cortisol). In addition to these, small amounts of sex hormones are secreted from the adrenal cortex. Normally these are unimportant but in certain abnormalities they can be secreted in extreme quantities and cause masculinizing effects.

To understand the many uses of corticosteroids, the underlying physiology governing their use, the bases of their adverse effects and the nursing implications to minimize or prevent these effects, it is important for nurses to have a working knowledge of the normal physiology of the adrenal cortical steroids.

Mineralocorticoids include aldosterone, corticosterone (also has glucocorticoid properties) and deoxycorticosterone, with the aldosterone accounting for more than 90 percent of mineralocortocoid activity. The basic actions of the mineralocorticoids are to increase renal tubular reabsorption of sodium and renal excretion of potassium. There are several factors regulating the secretion of aldosterone. Of these, potassium ion concentration and the renin-angiotensin system are by far the most potent.

Glucocorticoids include cortisol and corticosterone with cortisol accounting for about 95 percent of all glucocorticoid activity. By far, the primary effects of cortisol are those directly related to carbohydrate, protein and fat metabolism.

The release of glucocorticoids causes an increase in gluconeogenesis in the liver. Gluconeogenesis results from cortisol increasing enzymes that are required to convert amino acids into glucose in the liver cells. Glucocorticoids also encourage glycogen synthesis in the liver and stimulate the release of insulin.

Glucocorticoids affect protein metabolism by decreasing protein synthesis and increasing protein catabolism in all body cells except the liver. The extrahepatic catabolism of proteins mobilizes amino acids that serve as a source for gluconeogenesis in the liver. In Mary's case, this caused significant muscle wasting in her lower extremities. Glucocorticoids affect fat metabolism by promoting mobilization of fatty acids from adipose tissue.

Generally, these metabolic functions of the glucocorticoids are to help the body respond to stress and change. With increased demands, more cortisol is secreted and gluconeogenesis is initiated: the liver is stimulated to raise the blood sugar, the body's response to inflammation is modified and fluid balance is controlled. In fact, during extreme periods of stress, cortisol secretion can cause a six- to 10-fold increase in gluconeogenesis.


Corticosteroids: Management of Iatrogenic Cushing's Syndrome

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